Practice Question Review

Pts. with down syndrome have a 10-20x greater risk of?

Acute lymphoblastic leukemia

Candida albicans is a?

Budding yeast with pseudohyphae and germ tube

A KOH (potassium hydroxide) prep can be used to identify?

Candida Albicans

What agent causes yeast infections?

Candida albicans, which also causes vulvovaginitis ("yeast infection") and diaper rash in babies. Candida vulvovaginitis accounts for approximately 1/3 of vaginitis cases, and C. albicans accounts for 80-90% of those cases.

Ataxia and seizures with hypotonia, hepatosplenomegaly, microcytic hypochromic anemia, neutropenia and fragile silver colored hair indicates?

Deficiency in Copper This patient is presenting with Menke kinky hair syndrome due to a deficiency in copper. This presents as fine fragile silvery hair, depigmentation of the skin, muscle weakness, neurological abnormalities, and hepatosplenomegaly. A deficiency in copper results in osteoporosis due to defective collagen. It is also associated with skin depigmentation due to dysfunctional melanin synthesis from the copper-dependent enzyme tyrosinase. A copper deficiency also results in a microcytic, hypochromic anemia and neutropenia.

What is the lifecycle of hep B?

Mature virion = dane particle Replication of genome occurs within newly synthesized capsid through reverse transcriptase from RNA template *Mature capsid contains partially double stranded circular DNA and reverse transcriptase*

Thayer-Martin media is designed to grow?

Neisseria gonorrhoeae

What oxidase-positive gram neg rod is found in water? What sugars does it ferment?

Pseudomonas Does not ferment any sugars *Burn victims* Bottom Line: Pseudomonas aeruginosa is found ubiquitously in water. Common associations include hot tub folliculitis, otitis externa, eye infections in contact lens users, cellulitis in burn victims, and pneumonia in cystic fibrosis.

What can be used to Tx toxoplasmosis?

Pyrimethamine and sulfadiazine

What can be given for meningitis prophylaxis?

Rifampin

What is a catalase negative bacitracin sensitive cocci?

Strep pyogenes

What does shigella toxin and enterohemorrhagic e. coli have in common?

Stx-1 (VT1) can inhibit protein synthesis and is related to shiga toxin Protein synthesis inhibition by inhibiting 60S ribosome

What complement deficiency predisposes a patient to Neisseria infection?

Terminal complement: C6-9 Meningococcal disease describes infections caused by the bacterium Neisseria meningitidis (also termed meningococcus). It carries a high mortality rate if untreated. While best known as a cause of meningitis, widespread blood infection (sepsis) is more damaging and dangerous. Meningitis and meningococcemia are major causes of illness, death, and disability. Symptoms of meningococcemia are, at least initially, similar to those of influenza. Typically, the first symptoms include fever, nausea, myalgia, headache, arthralgia, chills, diarrhea, stiff neck, and malaise. Later symptoms include septic shock, purpura, hypotension, cyanosis, petechiae, seizures, anxiety, and multiple organ dysfunction syndrome. In severe fulminant meningococcemia, disseminated intravascular coagulation, adrenal hemorrhage and adrenal failure (Waterhouse-Friderichsen syndrome) may present as complications. Waterhouse-Friderichsen syndrome (WFS) (hemorrhagic adrenalitis, fulminant meningococcemia) is defined as adrenal gland failure due to bleeding into the adrenal glands, caused by severe bacterial infection (most commonly the meningococcus Neisseria meningitidis). The bacterial infection leads to massive hemorrhage into one or (usually) both adrenal glands. It is characterized by overwhelming bacterial infection meningococcemia leading to massive blood invasion, organ failure, coma, low blood pressure and shock, disseminated intravascular coagulation (DIC) with widespread purpura, rapidly developing adrenocortical insufficiency and death. An increased susceptibility to infection is a common clinical finding in most patients with complement deficiencies. The kinds of infections relate to the biological functions of those components that are missing. Activation of complement in the fluid phase can occur through the classical, lectin, or alternative pathway. Deficiencies of components of the classical pathway lead to the development of autoimmune disorders and predispose individuals to recurrent respiratory infections and infections caused by encapsulated organisms, including Streptococcus pneumoniae, Neisseria meningitidis, and Hemophilus influenza. The presence of serum bactericidal IgG and IgM is probably the most important host factor in preventing invasive disease. These antibodies are directed against both capsular and non-capsular surface antigens. The antibodies are produced in response to colonization with strains of N. meningitidis. The role of bactericidal antibodies in prevention of invasive disease explains why high attack rates are seen in infants from 6 to 9 months old, the time at which maternal antibodies are being lost. Individuals with complement deficiencies (C5, C6, C7, or C8) may develop meningococcemia despite protective antibody. C7 plays a critical role in the hydrophilic-amphiphilic transition because it confers on the intermediate complex C5b-7 the transient ability to bind directly to target cell membranes. The membrane-bound C5b-7 complex facilitates the incorporation of a C8 molecule and subsequently several C9 molecules into the membrane attack complex resulting in formation of a poly-C9 transmembrane pore. This emphasizes the importance of the complement system in defense against meningococcal disease.

What mediates anaphylaxis?

The patient is most likely having an anaphylactic reaction to the bee sting as evidenced by the difficulty breathing and the body rash. The fact that these symptoms occurred almost immediately after the bee sting suggests the boy had been stung previously and had produced IgE antibodies. Anaphylactic reactions are systemic type I hypersensitivity reactions that involve degranulation of mast cells and basophils. In a sensitized individual, the first step in an anaphylactic reaction is binding of the antigen to IgE antibodies. These IgE antibodies are synthesized prior to the anaphylactic reaction, and are found on the surface of mast cells and basophils, which both have Fc epsilon I receptors. These receptors bind the constant region of the IgE antibodies, allowing the antigen binding sites to be available. Antigen cross-links 2 IgE antibodies, resulting in release of histamine and other vasoactive compounds. These mediators produce the symptoms of anaphylactic response by inducing vasodilation and smooth muscle contraction. These responses occur very quickly following contact with the antigen because the antibodies are already bound to the mast cells.

What residue is targeted by penicillin?

Transpeptidases and thus cell wall linkage D-alanine-D-alanine is targeted

What is the only glycosylated HIV polyprotein?

gp160 from *env* Glycosylated in the rough ER and golgi *Becomes* gp41 and gp120 - act to evade immune cells and bind host cells

What is the inheritance pattern of PKU?

*Auto recessive* This child's diagnosis is phenylketonuria (PKU) which manifests with failure to thrive, mental retardation, microcephaly, large facial bones, gapped teeth, enamel defects, eczematous rash, hyperreflexia, increased muscle tone, fair skin, urine with a "mousy" odor, and, most notably, elevated serum phenylalanine. The disease is caused by a defect in the metabolism of phenylalanine which is normally converted to the amino acid tyrosine by phenylalanine hydroxylase. This means in patients with PKU tyrosine is an essential amino acid. PKU is inherited in an autosomal recessive fashion. This fact, and the fact that neither parent has the disease, implies that both parents are heterozygous carriers [Rr]. Thus, 25% of their children will be unaffected [RR] and 25% will also be affected [rr], while 50% will be heterozygous carriers [Rr] like the parents

What viruses are susceptible to the environment and alcohol rubs?

*Enveloped viruses* - flu, HIV, herpes Dissolves lipid bilayer

What mediates Staph scalded skin syndrome?

*Exotoxins* from staph

What GI bug may show neuro deficits after infection? What is this called?

*Guillain Barre syndrome* *Campylobacter jejuni* Thought to be caused by molecular mimicry that causes demyelination in peripheral nerves

What condition can interfere with CRP production?

*Liver disease - cirrhosis* C-reactive protein (CRP) is an acute phase reactant that is produced during inflammation. CRP is also important in assisting the binding of complement to damaged cells and microbial pathogens, thus aiding in the defense against acute infections. The liver is responsible for the production of many vital proteins, such as albumin, acute phase reactants including CRP, and clotting factors. Liver damage interferes with these secretions

Where do anticholinergics work?

*NOT* at nicotinic junction of NMJ but at *muscarinic receptors for ACh in PNS*

What enzyme is missing in Tay Sachs?

A deficiency in hexosaminidase A causes Tay-Sachs disease. The deficiency leads to an accumulation of gangliosides in the lysosomes of the central nervous system. Specifically, the accumulation is of GM(2)-gangliosides. Normal amounts of GM(2)-gangliosides comprise 1-3% of central nervous system gangliosides. Patients with Tay-Sachs can accumulate amounts up to 90% of central nervous system gangliosides. Clinical characteristics include mental retardation, paralysis, motor deterioration, blindness, and a cherry red macula.

What is the pathophysiology of Tay-Sachs?

A deficiency in hexosaminidase A causes Tay-Sachs disease. The deficiency leads to an accumulation of gangliosides in the lysosomes of the central nervous system. Tay-Sachs disease is classified as a sphingolipidoses, a type of lysosomal storage disorder. Along with Tay-Sachs, the other diseases in this classification include Niemann-Pick, Gaucher's, Krabbe's, Fabry's, and Metachromatic Leukodystrophy. Sphingolipids and fatty acids make up the myelin sheath, the insulator of the nerve fibers in the central nervous system. Sphingolipidoses are disorders marked by enzyme deficiencies that lead to abnormal accumulation of sphingolipids secondary to inability to metabolize or destroy them. The primary site this occurs is in the cellular lysosomes. All but Fabry's Disease lead to serious central nervous system disruption and result in varying degrees of mental retardation. The pathway to create sphingolipids begins with Serine + Palmitoyl CoA to create a sphingosine. When a fatty acid is added to a sphingosine, a ceramide is created. Ceramides are used to create both sphingomyelin and cerebrosides. When choline is added to a ceramide sphingomyelin is created. When a sugar is added to a ceramide, a cerebroside is created. When N-acetylneuraminic acid is added to the cerebroside a ganglioside is created. Gangliosides are broken down via hexosaminidase A, the enzyme that is deficient in Tay Sachs leading to abnormal accumulation of gangliosides.

How does acetaminophen work? Does it act on thromboxanes?

Acetaminophen is a pain reliever and fever reducer. Fever reduction is achieved by reducing the production of prostaglandins which mediate the fever response Does *NOT* act on thromboxanes - *ASA* does

A child with a brassy, barking cough may have?

Acute laryngotracheitis (croup) from *paramyxoviruses* specifically *parainfluenza virus*

Where does streptomycin function?

Aminoglycoside 30S ribosomal subunit

What causes bacterial vaginosis? Tx?

Anaerobic gram-variable rod *Gardnerella vaginalis* *Clue cells are seen* with *fishy odor* and *no inflammation* Metronidazole or clindamycin

What common GI parasite shows chest radiograph indicates several rounded infiltrates scattered throughout the lung fields bilaterally. Sputum analysis reveals Charcot-Leyden crystals and eosinophils.

Ascaris lumbricoides is one of the most common intestinal roundworm parasites found in the world, especially in developing nations. Infection occurs when eggs are ingested via the fecal-oral route. This occurs most commonly by improperly prepared food or unwashed hands. Many times, the infection is asymptomatic. However, pulmonary symptoms can arise when the larvae migrate through the lungs. This disease is often associated with an eosinophilic pneumonitis, in which patients may experience a non-productive paroxysmal cough, dyspnea, wheezing, and chest pain. Histologically, a lung biopsy will show lung infiltrated with large amounts of eosinophils. Chest radiography may demonstrate bilateral nodular opacities. Radiographic evidence is present in approximately 80% of the patients who progress to eosinophilic pneumonitis. The Charcot-Leyden crystals (which appear as hexagonal, slender crystalloids) are byproducts of the hyper-production of eosinophils. Other potential complications that can arise are intestinal obstruction, malnutrition, biliary colic, or migration to ectopic sites including the mouth, nose, and lacrimal ducts. One hallmark of the disease is being able to visualize the large round eggs under microscopy from a stool sample. Treatment for this infection includes albendazole, mebendazole, or pyrantel pamoate. The life cycle of Ascaris includes: ingestion of the egg; hatching within the small intestine; the larvae burrow out of the intestines and enter into the venous circulatory system where they travel through the liver and heart and end up in the lungs. The larvae break through the alveoli and ascend the tracheobronchial tree. They are then swallowed and return to the intestines where they develop into adults. After mating, eggs are released in the stool. Although most individuals infected by Ascaris are asymptomatic, 2 primary sites of pathology are possible in the lungs due to a hypersensitivity reaction to the larvae and in the gastrointestinal tract if there is a relatively large worm burden that causes obstruction/perforation of the intestines. In children, the adult worms can also cause malnutrition. Below are images of the eggs or larvae of other parasitic worm pathogens that may be in a differential diagnosis for an Ascaris infection. Bottom Line: Ascaris lumbricoides is a parasitic infection that occurs from ingestion of undercooked food. Patients can develop pulmonary symptoms; round infiltrates can be found on chest radiograph, and large round eggs are seen with microscopy of stool samples.

What cells are most commonly malignant in chronic and acute lymphocytic leukemia?

B-cells are the most common malignant cells of both chronic and acute lymphocytic leukemia. Immunophenotypic analysis often reveals a clonal population of cells that express B-cell associated antigens (CD19, 20, 23), T-cell associated antigens (CD5), and low levels of surface immunoglobulin. Morphologically, CLL cells resemble mature small lymphocytes, but they are clonal B cells arrested in the B cell differentiation pathway at some intermediate step between pre-B cell and mature B cell. The majority of CLL cases exhibit B cell leukemia/lymphoma 2 (BCL2) expression, a proto-oncogene which suppresses apoptosis.

Where does botulism act? What form can it take?

Blocks vesicle release/exocytosis Cleaves SNARE proteins Spore-forming, gram + anaerobe

What is seen in multiple myeloma? Tx?

Bone pain, fatigue, anemia, kidney disease and hypercalcemia Neoplastic B cells mature into plasma cells that generate XS Ig - susceptible to proteasome inhibitors like boretezomib, a boronic acid containing dipeptide = *apoptosis*

Pelvic examination reveals severe cervical inflammation and a foul-smelling, thick, green, frothy discharge in the vaginal vault:

Bottom Line: A sexually active female with a frothy, foul-smelling greenish discharge should be suspected of having a Trichomonas vaginalis infection. The organism is a motile protozoan. Thick, green discharge that is foul-smelling. This is the classic presentation of Trichomonas vaginalis. The cervical inflammation caused by T. vaginalis is often referred to as strawberry cervix. Trichomonas vaginalis is a motile protozoan that is transmitted sexually

What agent is used to treat trichomonas vaginalis? MoA?

Bottom Line: Metronidazole is the drug of choice in treating infections caused by Trichomonas vaginalis. Its mechanism of action is to damage DNA through the production of free radicals inside bacteria and protozoa. The most effective treatment against Trichomonas vaginalis is metronidazole. Metronidazole is a bactericidal and an antiprotozoal medication indicated for the treatment of Trichomonas, Giardia, Entamoeba, Gardnerella vaginalis, and anaerobes (Bacteroides, C. difficile). And is used with a proton pump inhibitor and clarithromycin for "triple therapy" for H. pylori. Its mechanism of action is the formation of free radical toxic metabolites in bacterial and protozoal cells that irreparably damage DNA and lead to cell death

What is african river blindness?

Bottom Line: Onchocerciasis, also known as river blindness, presents 9-12 months after being infected with the parasite by the bite of a black fly and can lead to irreversible blindness. The patient is most likely suffering from onchocerciasis, which is an infection caused by Onchocerca volvulus. This parasite is transmitted by the black fly, which is found in Africa, Yemen, and parts of South America. The majority of cases are found in the continent of Africa and it is the second-leading infectious cause of blindness worldwide (after trachoma caused by Chlamydia trachomatis serotypes A-C). When a human is bitten by the black fly, the fly transmits the parasitic larvae into the bloodstream of the human. Click the following link for a complete life cycle by the CDC (http://www.cdc.gov/dpdx/). After infection, the larvae grow to adult worms within the bloodstream and lymphatics. The adults embed into the skin, forming subcutaneous nodules and bear microfilarial offspring which invade the eye and its inner chambers. Overall, these offspring cause eye pain, redness, iritis, and anterior uveitis in the patient. These microfilarial worms disseminate throughout the body, causing an allergic-type reaction and a skin condition known as onchodermatitis. This disease is also known as river blindness because the black flies live near the rivers and the native tribes realized that the individuals who went down to the rivers were the only people in the village who would eventually go blind. The treatment of choice for this disease is an antiparasitic ivermectin.

Tx for beta-hemolytic gram-positive cocci that are catalase-negative and sensitive to bacitracin?

Bottom Line: Penicillin is the first-line treatment for group A strep (Streptococcus pyogenes), which is beta hemolytic (complete hemolysis), bacitracin sensitive, and catalase negative. Rapid antigen detection test has a sensitivity between 70-90%. This boy has strep throat caused by Streptococcus pyogenes (group A strep or GAS). All streptococcus species are catalase-negative, and S. pyogenes is beta-hemolytic (clear hemolysis) and sensitive to bacitracin. Streptococcus agalactiae (group B strep) is bacitracin resistant. When a child presents with pharyngitis, you must determine if GAS is the cause in order to prevent the overuse of antibiotics, reduce severity and duration, and prevent suppurative complications and acute rheumatic fever. Rapid antigen detection test and/or throat culture should be performed on patients with erythema, edema, and/or exudates and absence of signs of viral infections, signs of GAS infection (scarlatiniform rash, palatal petechiae, pharyngeal exudate, vomiting, tender cervical nodes), or exposure to GAS. Rapid antigen detection tests for streptococcus have a sensitivity of 70-90% and specificity of 90-99%. Due to the high specificity, but limited sensitivity, a positive RADT is establishes the diagnosis of GAS, but a negative RADT does not rule out GAS. RADT can miss as many as 30% of cases; therefore, a throat culture should be performed if the patient has a negative RADT. The sensitivity of a throat culture is 90-95% for GAS. Penicillin is the drug of choice used to treat group A strep infections.

What UTI cause is catalase-positive, coagulase-negative, gram-positive cocci in clusters and has novobicin resistance?

Bottom Line: The second most likely cause of urinary tract infections in sexually active young women is Staphylococcus saprophyticus, a gram-positive coccus that is catalase-positive, coagulase-negative, and resistant to novobiocin. The most common cause of UTI's in this group is E. coli. However, the urine nitrites (negative) and gram staining reaction (gram-positive cocci) indicate that this patient's current condition is due to S. saprophyticus, not E. coli. The patient's symptoms of dysuria, increased frequency, and lower abdominal pain are clues to a urinary tract infection (UTI). The urinalysis reveals a cloudy specimen (a clue to pyuria) and positive leukocyte esterase, both consistent with a UTI. The most common cause of UTI's in young sexually active females is Escherichia coli. However, E. coli is positive for urine nitrites. This patient's urine nitrites are negative. So the cause of this patient's UTI is not due to the most common cause but rather, to the second most common cause of UTI's in young sexually active females: Staphylococcus saprophyticus. S. saprophyticus is a catalase-positive, coagulase-negative, gram-positive cocci in clusters. Since it does not produce coagulase it is placed with several other species of staphylococci called the coagulase-negative staphylococci, or CoNS. To differentiate S. saprophyticus from the other CoNS species, a novobiocin resistance test is performed. S. saprophyticus is resistant to novobiocin. Other CoNS species, like Staphylococcus epidermidis, are novobiocin sensitive. S. saprophyticus is nonhemolytic (gamma hemolytic) on blood agar plates. Osteopathic findings can include viscerosomatic reflexes for the lower urinary tract as TART changes from T11-L1. There may also be pelvic diaphragm dysfunction as a result of local inflammation due to the urinary infection.

How is protozoan vaginosis (Trichomonas vaginalis) tesed for?

Bottom Line: Trichomonas vaginalis is an STD caused by a motile protozoan. Several diagnostic tests are available to aid in the detection of T vaginalis including nucleic acid amplification test (gold standard), culture, and direct microscopic visualization on a wet mount slide.

Acetaminophen can cause what variety of liver damage?

Centrilobular necrosis Acetaminophen is metabolized in the liver, where toxic levels can deplete glutathione stores and allow the accumulation of free radicals. Damage to the hepatocytes by these free radicals causes centrilobular as well as diffuse necrosis in the liver. This damage, if left unchecked or untreated, eventually leads to liver failure, the most common cause of death due to an acetaminophen overdose

What leukemia is most commonly found in men over 60?

Chronic lymphocytic leukemia (CLL) is the most common type of leukemia found in men over the age of 60. An elevated white blood cell count, anemia, and lymphadenopathy are classic findings. The onset is insidious and commonly detected in asymptomatic patients with an unexplained elevated white blood cell count. The peripheral smear shows an excess of mature lymphocytes. In the lower right corner, there is a smudge cell, which is classic for CLL.

What autosomal recessive disorder shows lysosomal transport protein defect and recurrent bacterial infections?

Chédiak-Higashi syndrome is a rare autosomal-recessive disorder caused by defects in the lysosomal transport protein, LYST, and is characterized by recurrent bacterial infections, partial oculocutaneous albinism, photophobia, nystagmus, and peripheral neuropathy. The immunodeficiency is caused by the dysfunction of lysosomal granules of leukocytes and manifests as increased susceptibility to bacterial infection. Many patients die in childhood from recurrent infections. An aggressive lymphoproliferative phase develops in about 50% of the patients surviving into adolescence. The diagnosis of Chédiak-Higashi syndrome is easily made by inspection of the peripheral smear for giant lysosomes or microscopic examination of hair for characteristic melanin clumps. PLAIN: Progressive neurodegeneration, Lymphohistiocytosis, Albinism (partial), recurrent pyogenic Infections by staphylococci and streptococci, peripheral Neuropathy

What is the t1/2 of drugs with first order kinetics?

Constant The patient is taking methotrexate which follows first-order kinetics, like most drugs. The half-life (t1/2) of a drug can be calculated by the following equation: 0.7 x Vd/Cl, where Vd is defined as the volume of distribution and Cl is clearance of the drug. This indicates that the half-life is constant regardless of the dose because neither the volume of distribution (Vd) nor the clearance (Cl) changes with dose. The half-life is the time it takes to eliminate 50% of the drug. In first-order kinetics the rate of elimination is directly proportional to drug concentration and a constant fraction of drug is eliminated per unit time

What is the primary cause of subacute endocarditis in patients with dental caries and gingivitis?

Due to the newly diagnosed heart murmur and poor oral hygiene, this patient most likely has subacute endocarditis caused by Streptococcus mutans. S. mutans is an alpha-hemolytic or non-hemolytic, optochin-resistant (non-sensitive) Gram-positive coccus that is a normal flora of the oral cavity but can cause dental caries and gingivitis in patients who have poor oral hygiene. When the gums pull away from the teeth and bleed, this can allow S. mutans to access the bloodstream and spread hematogenously to the heart. S. mutans then can then colonize the heart valves, leading to chronic inflammation with possible low-grade fevers, fatigue, weight loss, back pain, and murmurs. One major reason that S. mutans is a primary cause of subacute endocarditis is that these bacteria can form biofilms on the heart valves, which inhibit the function of antibodies, antibiotics, and immune cells.

What is a Gram-negative, lactose fermenting bacilli?

E. coli

What GI bug ferments sorbitol?

Enteroinvasive e.coli - EIEC Escherichia coli can manifest as various types of diarrhea depending on which strain and virulence factor is present. In the case of the question above, bloody diarrhea with white blood cells and fever is consistent with enteroinvasive E coli (EIEC). The presentation is similar to mild Shigella dysentery because the main virulence factor that allows the bacteria to invade is encoded in a plasmid that is shared by Shigella and pathogenic E coli. The bloody diarrhea is a result of direct invasion of the bacteria into the gastric mucosa (hence the name Enteroinvasive), which can lead to an immune-mediated inflammatory reaction causing fever. In addition, white blood cells, specifically neutrophils, migrate to the intestinal wall to clear the infection, so stool studies often show white blood cells. EIEC is grown on MacConkey agar and will ferment sorbitol. The condition is self-limiting, so treatment consists of fluid and electrolyte replacement. Out of all the answer choices, EIEC is the only one that causes both fever and bloody diarrhea. E coli is a Gram-negative facultative anaerobic rod that is a common inhabitant of the intestinal tract. It grows on MacConkey agar and is able to ferment lactose. Most of the E coli strains can ferment sorbitol, except for enterohemorrhagic E coli (EHEC), which is sorbitol negative (the agar to assess sorbitol fermentation is a variation of MacConkey agar and is called S-MAC). Due to gene transfer mechanisms, there are a variety of strains/serotypes/pathotypes of E coli, some of which are associated with intestinal pathology. Out of the main pathogenic E coli associated with intestinal tract disease, EHEC is endemic in the United States. Most of the other pathotypes are generally acquired through travel. Another common feature is that most of these are associated with self-limiting infections. Bottom Line: Enteroinvasive Escherichia coli causes a bloody diarrhea with white blood cells in the stool and fever due to the immune-mediated inflammatory reaction.

What is a field defect?

Example is holoprosencephaly Initial embryonic disturbance causes multiple malformations by effecting surrounding tissues

Child with thin upper lip, microcephaly and small palpebral fissures mau have?

FAS

What enables flu-host interaction?

Flu is (-) sense RNA that is enveloped in host plasma membrane Hemagglutinin surface membrane = surface glycoprotein for interaction

Antidote for benzodiazepines?

Flumazenil Benzo receptor antagonist

Antidote for ethylene glycol?

Fomepizole or ethanol

What agent can cause septic arthritis and has gram negative coccobacilli that requires hematin and NAD+ to grow?

H. Influenzae Localized infections are caused by uncapsulated strains but type b infxn can be seen in unvaccinated pts. causing invasive disease Type b has a *antiphagocytic polysaccharide capsule* -> septic arthritis and meningitis

What has a positive monospot test?

HHV4 EBV

What enables recurrent N. gonorrhea infections?

High variability of surface antigens

What CD factors are found on Reed-Sternberg cells?

Hodgkin's lymphoma cells CD 15 and 30

What is the triad for congenital toxoplasmosis?

Hydrocephalus, intracranial calcifications and chorioretinitis *In-utero infection*

CSF in meningitis patients most likely show what characteristics? What is the most common cause of bacterial meningitis?

Increased opening pressure, increased neutrophils, increased protein, decreased glucose Strep pneumoniae most common Gram + cocci in pairs

Most common causes of epididmyitis and treatment?

Infections with urinary coliforms such as Escherichia coli, Pseudomonas aeruginosa, Proteus spp., and Klebsiella spp. are the most common cause in children and in men older than 35 years of age. Chlamydia trachomatis serotypes D-K is the most common cause in sexually active men younger than 35 years of age. Infections with Neisseria gonorrhoeae and Treponema pallidum also occur in this population. Treatment is with the combination of ceftriaxone + doxycycline or ceftriaxone + azithromycin because of the high incidence of co-infection with both chlamydia and gonorrhea. Chlamydia trachomatis. Treatment is with the combination of ceftriaxone and doxycycline because of the high incidence of co-infection between chlamydia and gonorrhea.

dark field microscopy is used for?

It is useful in analyzing spirochetes, such as Treponema pallidum in the diagnosis of syphilis

What is seen in neonatal vitamin K deficiency?

K is cofactor for gamma-glutamyl carboxylase - carboxylation is needed for clotting factors 2, 7, 9 and 10 to create calcium binding sites *Babies often given post-natal vitamin K*

What respiratory infection can show XS neutrophils but no organisms?

Legionella pneumoniae

What agent are intracellular gram + rods that produce narrow beta hemolysis and can grow in cold environments?

Listeria *Cell mediated response* Cytotoxic T-cells

Where do medial and lateral portions of the lower extremity drain lymphatically?

Medial and lateral tracks - medial bypasses popliteal and cause inguinal lymphadenopathy Lateral foot issues cause both

Gentamicin ADRs? Where does it act?

MoA: 30S and 50S ribosomal subunit Gentamicin is an aminoglycoside that could be toxic to the kidney. The two most common side-effects of aminoglycosides are ototoxicity and nephrotoxicity.

This patient presents with a low-grade fever, dry cough, and chest radiograph findings of bilateral interstitial infiltrates suggestive of an atypical pneumonia. This is most commonly due to?

Mycoplasma pneumoniae It is common in all age groups but most common in the first 2 decades of life and has the highest rate in patients 5-20 years of age. It is most common among school-aged children, military recruits, and college students due to the close living quarters and close contact that is needed to spread the infection via respiratory droplets. Infection occurs most frequently during the fall and winter. M pneumoniae is a short rod, considered to be the smallest organisms able to survive on their own, and is not able to be Gram stained due to its lack of a cell wall Bottom Line: Mycoplasma pneumoniae causes an atypical pneumonia, with an insidious onset of low-grade fever, non-productive cough, and diffuse interstitial infiltrates on plain film chest radiographs. *IgM cold agglutination* It can be diagnosed with the demonstration of a serum cold IgM agglutinin antibody. IgM antibodies to the antigen on erythrocyte membranes appear during the course of infection and produce cold agglutinins over the course of 1-2 weeks after infection. The incidence of cold agglutinins is highest in children and decreases with age. Treatment of choice is with azithromycin. M pneumoniae is a fastidious organism that requires specialized media for culture.

What is a complication of diptheria and how is it prevented?

Myocarditis/neuro toxicity *DPT vaccines makes IgG Ab*

What is the most common cause of viral gastroenteritis?

Norovirus Diarrhea, *vomiting*, fever, malaise and headache Watery diarrhea without blood or mucous

Where can histoplasma capsulatum be contracted and how does it present?

Ohio + Mississippi river valleys *Cave exploration* - bird or bat shite Ovoid yeast within macrophages Hilar and mediastinal lymphadenopathy and cough/fever/malaise

Antidote for anticholinergic OD?

Physostigmine - *Tx for OD of atropine and/or ipratropium which block acetylcholine

Tx for pseudomonas?

Piperacillin and ticarcillin are broad spectrum penicillins with activity against Pseudomonas aeruginosa. They are often combined with β-lactamase inhibitors, such as tazobactam, since they are not resistant to penicillinases. Like all penicillins, piperacillin inhibits the formation of the bacterial cell wall by inactivating the penicillin-binding protein, preventing the cell wall residues from cross-linking.

Antidote for heparin?

Promatine sulfate

What does the HIV pol gene do?

Protease, reverse transcriptase and integrase Mutes may indicate inconsistent medication use

What is a Coagulase-positive, β-hemolytic cocci?

Staph aureus

Artificial heart valve pts. may have infection from?

Staph epidermis - gram + coccus that is coagulase negative and is susceptible to novobiocin

What is a Coagulase-negative, novobiocin-resistant cocci?

Staph saprophyticus

What often causes acute otitis media?

Strep pneumo - haem influ - moraxella This patient has acute otitis media (AOM) which can be determined from the physical exam findings of a red, bulging, and non-mobile tympanic membrane. The development of point tenderness over the posterior aspect of the temporal bone points to the progression of AOM to mastoiditis. Mastoiditis is an infection of the mastoid air cells which is part of the temporal bone of the skull. It is usually caused by delayed treatment of otitis media and can progress further to cause meningitis. Antibiotic treatment must be initiated early in the treatment of otitis media. AOM is most commonly caused by Streptococcus pneumoniae or Haemophilus influenzae (nontypeable strain), followed in frequency by Moraxella catarrhalis. Since Streptococcus pneumoniae is not listed in the above choices, the correct answer is Haemophilus influenzae.

What can cause struvite stones?

Struvite stones are associated with urinary tract infections (UTIs) by urease-positive, gram-negative rods that are capable of splitting urea into ammonium, which then combines with phosphate and magnesium to form a crystal. Usual urease-positive etiologies include Proteus and Klebsiella species. Urine pH is typically greater than 8 due to the increased levels of ammonium in the urine. These patient's UTIs typically do not resolve until the stone is removed entirely, and the stone may develop into staghorn calculi within weeks to months without treatment.

Physical examination reveals cherry red spots on the macula and progressive developmental delay in Ashkenazi pt:

Tay-Sachs disease is an autosomal recessive disorder classified as sphingolipidoses, a type of lysosomal storage disorder. Along with Tay-Sachs, the other diseases in this classification include Niemann-Pick, Gaucher's, Krabbe's, Fabry's, and Metachromatic Leukodystrophy. All are autosomal recessive except for Fabry's disease, which is X-linked recessive. Tay-Sachs is most prevalent in Ashkenazi Jewish descent and results from a deficiency in the enzyme hexosaminidase A. The deficiency leads to accumulation of gangliosides in the lysosomes of the central nervous system. There are multiple subclasses of Tay-Sachs with variable age of onset and severity. Infantile onset is characterized by normal development until about 5 months of age where relentless neurodegeneration results in death around the age of 5 years. Characteristics include a decline in gross motor skills, paralysis, mental retardation, and blindness. The child will have delays in motor skills such as playing with toys and walking. Hyperacusis, a heightened startle response, is noted secondary to blindness as well as decreased eye contact. A key fundoscopic physical exam finding is cherry red spots on the macula of the patient. Bottom Line: Tay-Sachs disease is an autosomal recessive lysosomal storage disorder that most commonly occurs in Ashkenazi Jewish descent. Clinical characteristics of the disorder include a decline in gross motor skills, paralysis, mental retardation, and blindness. A common physical exam finding is a cherry red macula seen on fundoscopic exam.

Where is TB seen in the lung?

The Ghon complex (caseous necrosis) of primary TB favors the upper part of the lower lobe, and lower part of the upper lobe. Since none of these primary TB sites was offered as answer options, we must conclude that the patient has secondary TB, which preferentially affects the apices (and was offered as an answer choice). The lung apex is a commons site of growth because M. tuberculosis is an obligate aerobe and prefers the higher oxygen pressure found there, especially the right apex which has the highest oxygen pressure of all regions. The cavitary lesions of secondary TB are caused by the release of cytokines from memory T cells. Bottom Line: Adults from susceptible populations will most commonly present with secondary or reactivation TB, which prefers to grow in the lung apices. Symptoms can include weight loss, fevers, hemoptysis, and night sweats.

What artery supplies the lateral pons and cerebellum and can cause lateral pontine syndrome?

The anterior inferior cerebellar artery (AICA) supplies the lateral pons and lateral cerebellum, and occlusion causes lateral pontine syndrome. Clinical signs related to structures affected include nausea, vomiting, and vertigo (vestibular nuclei); facial paralysis, decreased lacrimation, and decreased salivation (facial motor nucleus); nerve deafness (cochlear nuclei); analgesia of ipsilateral face (spinal trigeminal nucleus); and analgesia of contralateral body (spinothalamic tract). These clinical signs are very similar to lateral medullary syndrome caused by occlusion of the posterior inferior cerebellar artery (PICA). What differentiates the 2 syndromes is that lateral pontine syndrome typically has facial paralysis and potentially nerve deafness, whereas lateral medullary syndrome does not. Instead, lateral medullary syndrome typically has uvula deviation (nucleus ambiguus), and lateral pontine syndrome does not. The clinical signs for this patient are consistent with lateral pontine syndrome.

How should CKD change dosage?

The equation for Maintenance Dose calculation is: Maintenance Dose = Cp x CL/F where Cp is the target plasma concentration, CL is the clearance, and F is the bioavailability. The bioavailability of a drug is 1 when it is given intravenously. The clearance of a drug can be mediated by filtration alone (inulin, where clearance = GFR) or filtration and complete secretion (para-aminohippuric acid where clearance = renal plasma clearance). The equation for Loading Dose is: Loading Dose = Cp x Vd/F where Cp is the target plasma concentration, Vd is the volume of distribution, and F is the bioavailability. The volume of distribution (Vd) is the volume of the total body fluid into which a drug appears to distribute. Standard values of volumes of fluid compartments in an average 70 kg adult are 3L plasma, 12L extracellular fluid, and 41L total body water. Notice that the Maintenance Dose equation contains the clearance (CL) which will be decreased in those with renal failure resulting in higher plasma levels. Drugs with a narrow therapeutic index may require dose adjustment. Since none of the variables in the loading dose equation is affected by renal or hepatic disease or dysfunction, the loading dose remains the same.

Cruise ship virus - GO!

The most common cause of gastroenteritis in adults is Norovirus, a single-stranded RNA virus that is highly contagious and transmitted by direct contact or fecal-oral routes. It causes blunting of the intestinal villi, which result in carbohydrate and fat malabsorption and leads to diarrhea. It also slows down gastrointestinal motility resulting in nausea and vomiting. It is the most common cause of outbreaks of gastroenteritis. Outbreaks occur in restaurants, schools, healthcare facilities, military barracks, and cruise ships, and are usually initiated by contamination of food by an infected food handler. These outbreaks can occur year round but are most common in the winter months. Symptoms develop 24-48 hours after exposure and can last from 24-72 hours. Symptoms include nausea and vomiting, watery diarrhea, mild fevers, abdominal cramps, headaches, and malaise. Treatment consists of fluid and electrolyte replacement, as well as antiemetics and analgesics when necessary. You may find viscerosomatic changes from T10-L2 representative of the small bowel and colon, along with restrictions in the suboccipital region as a result of parasympathetic changes. Because of the force of repeated vomiting, patients have some abdominal tenderness and often have restricted diaphragm from overworking the abdominal muscles and diaphragm.

What are the symptoms and Tx of organophosphate poisoning?

The patient has been exposed to Sarin gas, which is a man-made clear, colorless, odorless, tasteless gas used as a chemical weapon. Originally developed as a pesticide, sarin gas is an organophosphate compound which acts as a potent acetylcholinesterase inhibitor. The severity of symptoms depends on the degree of exposure which may occur through contact, ingestion, or inhalation. As with other forms of organophosphate toxicity, patients may present with "DUMBBELSS"- Diarrhea, Urinary incontinence, Miosis, Bronchospasm, Bradycardia, Excitation (central nervous system [CNS] excitation and skeletal muscle excitation), Lacrimation, Sweating, and Salivation. These adverse effects are caused by an abundance of acetylcholine in neuromuscular junctions of skeletal muscle as well as neuronal synapses of the autonomic nervous system. The clue to a potential bioterror attack lies in the fact that the patient and several others were exposed to a nerve agent in a large, public place. Prompt recognition and treatment may give the patients the most significant chance of survival. Of the answer choices, pralidoxime, which binds to organophosphates at nicotinic receptors and regenerates acetylcholinesterase, is the most appropriate pharmacologic agent for a suspected organophosphate poisoning. Atropine, which was not offered as an answer choice, is a muscarinic antagonist that competitively inhibits acetylcholine. In clinical practice, atropine would be given in conjunction with pralidoxime. Bottom Line: Patients exposed to the organophosphate, sarin gas, may present with diarrhea, urinary incontinence, miosis, bronchospasm, bradycardia, excitation of skeletal muscle, excitation of the central nervous system, lacrimation, sweating, and salivation. Pralidoxime regenerates acetylcholinesterase and is used in the treatment of acetylcholinesterase inhibitor toxicity.

What are major signs of endocarditis?

The patient is most likely exhibiting signs and symptoms of acute infective endocarditis on a prosthetic aortic heart valve. The valves may be damaged by autoimmune processes, from congenital mechanisms, or, most likely in this case, from surgery. Patients typically present with fever (occurring in 97% of patients), malaise, fatigue, a new change in heart murmur, septic embolism, Janeway lesions (painless hemorrhagic cutaneous lesions located on the palms and soles), splinter hemorrhages, Roth spots (emboli to the retinal vessels resulting in microinfarcts), and Osler nodes (painful subcutaneous lesions in the distal fingers). Prosthetic valve endocarditis (PVE) can arise early (within 2 months of implantation) or late (2 months after valve implantation) after surgery.

Acetaminophen OD and Tx?

These symptoms may include nausea or vomiting, sweating, loss of appetite, and diarrhea, as seen in this patient. In the next 24 to 48 hours, the early symptoms start to disappear, but liver damage starts to occur. Because of these potentially serious effects, early treatment after an overdose is important *N-acetylcysteine* Tx Damage to the liver, or hepatotoxicity, results not from acetaminophen itself, but from one of its metabolites, N-acetyl-p-benzoquinoneimine (NAPQI) (also known as N-acetyl iminoquinone). NAPQI depletes the liver's natural antioxidant glutathione and directly damages cells in the liver, leading to liver failure. Risk factors for toxicity include excessive chronic alcohol intake, fasting or anorexia nervosa, and the use of certain drugs such as isoniazid. Treatment is aimed at removing the acetaminophen from the body and replacing glutathione. Activated charcoal can be used to decrease absorption of acetaminophen if the patient presents for treatment soon after the overdose; the antidote acetylcysteine acts as a precursor for glutathione, helping the body regenerate enough to prevent damage to the liver. N-acetylcysteine can neutralize NAPQI by itself as well. A liver transplant is often required if damage to the liver becomes severe. Patients treated early have a good prognosis, whereas patients that develop major liver abnormalities typically have a poor outcome. Acetaminophen is a reversible cyclooxygenase inhibitor used to relieve fever and pain

What is primary central nervous system lymphoma?

This is a lymphoma seen mostly in adults, associated with HIV/AIDS and EBV. It is considered an AIDS-defining illness (if you have this you definitely have aids). There's variable presentation but symptoms include memory loss, confusion, seizures. Lab: you'll see masses in the brain, but need to look at CSF to distinguish this from toxoplasmosis gondii infection. *EBV often seen*

What is malignant hyperthermia? What is the Tx?

This patient has malignant hyperthermia. This is a rare, life-threatening condition triggered by inhaled anesthetics and the muscle relaxant succinylcholine. It is characterized by excess intracellular Ca2+ leading to uncontrollable muscle contractions. The extensive contractions deplete ATP, produce heat, and eventually damages the muscle cells. A genetic predisposition is related to mutations in the ryanodine receptor calcium channel which predisposes certain individuals to this condition. *Tx: Dantrolene is the drug of choice to treat malignant hyperthermia. It prevents calcium release from the sarcoplasmic reticulum.*

What infection shows umbilicated papules?

This patient has the characteristic molluscum contagiosum skin papules. Molluscum contagiosum is a self-limited epidermal infection caused by a Poxviridae family virus. It is characterized by flesh-colored, dome-shaped papules that are firm and umbilicated (shown below). These lesions commonly occur in children and sexually active adults, however, it is important to note that although it can be spread by sexual contact, molluscum contagiosum is not considered a sexually transmitted infection because it is transmitted by skin to skin contact. Kids in daycare settings or adolescents in team sports (i.e. basketball, wrestling) are at risk of acquiring and spreading the poxvirus harbored in these lesions due to frequent skin to skin contact. When biopsies of the papules are performed, eosinophilic cytoplasmic inclusion bodies are a typical finding. Typical presentation of Molluscum contagiosum

What should be used in pt. with peaked-T waves?

This patient has undergone a traumatic crush injury. This history, along with abnormal T-waves, suggest the patient is experiencing hyperkalemia. This metabolic abnormality can result in cardiotoxicity if not addressed promptly. Initial management includes several simultaneous measures. Calcium gluconate is often the first medication administered as a cardioprotective agent. It is essential for treatment involving cardiac symptoms, though it does not directly affect potassium levels. Medications that would improve hyperkalemia include β-adrenergic agonists (such as terbutaline or albuterol), insulin, and sodium polystyrene sulfonate (Kayexalate).

What respiratory infection is associated with the west/deserts?

This patient is experiencing acute respiratory distress syndrome (ARDS) as a result of a Hantavirus infection. This virus is found in the southwestern United States and this individual contracted it during his trip to the Grand Canyon. Transmission is typically via inhalation of contaminated rodent feces in the dry air. Patients with Hantavirus infections typically present with moderate to severe respiratory symptoms that quickly (within ~24 hours) worsen into ARDS, with possible hemorrhage and renal failure. Severe disease is characterized by a cardiopulmonary syndrome where fluid accumulation in the lungs puts pressure on the heart that can lead to congestive heart failure. Currently, there is no effective treatment and this infection has a high mortality rate.

What test can be used to diagnose Celiac disease?

This patient most likely has celiac sprue, resulting from antibodies against gluten, a protein found in wheat products. Patients suffering from this disease experience intestinal and extraintestinal symptoms. Intestinal symptoms may include diarrhea, steatorrhea, abdominal bloating, flatulence, and abdominal distention. Extraintestinal symptoms include microcytic anemia secondary to malabsorption of iron, weight loss, failure to thrive, dermatitis herpetiformis, transaminitis, and symptoms resulting from malabsorption of fat soluble vitamins (i.e. osteoporosis from malabsorption of vitamin D). This patient did have the intestinal symptom of new onset diarrhea within the past 2-3 months. This correlates to the start of table foods into her diet, of which gluten-containing products are likely to be present. Just as important are the extraintestinal manifestations in this patient, including failure to thrive and a microcytic anemia, of which iron deficiency is the most common cause due to malabsorption of iron. Testing for the antibodies can help sort out the differential, and serum levels of IgA antigliadin antibody, IgA tissue transflutaminase, and IgA endomysial antibody can be obtained. Diagnosis is confirmed by EGD with small bowel biopsy demonstrating flattened villi. A gluten-free diet can prevent these symptoms from occurring.

Tx for homocystinuria?

This patient most likely has homocystinuria, which is most commonly due to reduced activity of the enzyme cystathionine synthase. This enzyme is normally responsible for converting homocysteine to cystathionine, with the necessary cofactor of pyridoxine (Vitamin B6). Pyridoxine supplementation is proven to be helpful in many patients who have this inheritable enzyme deficiency. The other answer choices suggest the other, frequently confused B vitamins.

What is seen in neonatal meningitis?

This patient most likely has neonatal meningitis. Early onset neonatal meningitis usually presents in the first few days to week after birth, often in a premature infant. Symptoms can include fever, apnea, feeding difficulty, irritability, and lethargy. Neonatal meningitis is most commonly caused by group B streptococcus (Streptococcus agalactiae) passed to the child from its mother. The typical cerebral spinal fluid (CSF) findings in this bacterial meningitis include increased opening pressure on lumbar puncture, increased PMNs, increased protein, and decreased glucose.

Tx for infectious urethritis?

To cover both gonococcal (N. gonorrhea) and non gonococcal, Tx with doxycycline and macrolides (mycins) N. gon - ceftriaxone C. trach - macrolides and doxy

Northern vs. southern blot?

Transcription and translation are the underlying processes in gene expression. RNA is first transcribed from a DNA template and this messenger RNA (mRNA) is then translated into protein. Northern blots are used to detect the presence of an RNA molecule and its size. RNA molecules are first separated on size using gel electrophoresis. These RNA molecules are then transferred to a nylon membrane. To detect the RNA molecule of interest, a complimentary single-stranded DNA from which the RNA strand was transcribed, is incubated to the membrane. A probe bound to the RNA of interest then allows for detection of the specific molecule. A Northern blot is similar to a Southern blot, except that it involves a radiolabeled DNA probe binding to a sample of RNA. Bottom Line: A Northern blot is a technique useful in identifying a sample of RNA through its binding to a radiolabeled DNA probe. The standard screening assay for detecting antibodies to HIV is an enzyme immunoassay (EIA). A confirmatory Western blot is performed if the screening test is positive in order to exclude a false positive test.

Potassium may be released from what injuries?

Traumatic crush injuries result in massive tissue damage with necrosis of muscle. Muscle, as with all cells, has a large store of potassium that will be released. Additionally, creatine kinase, myoglobin, and phosphate levels will sharply elevate. The myoglobin will cause an acute kidney injury (AKI) due to acute tubular necrosis (ATN), known as crush syndrome. Crush syndrome may include hypovolemic shock, hyperkalemia, heart failure, arrhythmias, acute respiratory distress, sepsis, and/or disseminated intravascular coagulation (DIC). The characteristic manifestation of rhabdomyolysis is the dark-colored, pigment-induced urine due to loss of myoglobin in the urine.

Which AA becomes essential in PKU?

Tyrosine This child's diagnosis is phenylketonuria (PKU), which manifests with failure to thrive, mental retardation, microcephaly, large facial bones, gapped teeth, enamel defects, eczematous rash, hyperreflexia, increased muscle tone, fair skin, urine with a "mousy" odor, and, most notably, elevated serum phenylalanine. The disease is caused by a defect in the metabolism of phenylalanine which is normally converted to the amino acid tyrosine by phenylalanine hydroxylase. Because this patient lacks phenylalanine hydroxylase, tyrosine cannot be formed. It then, by definition, becomes an essential amino acid (one the body cannot produce that must instead be absorbed from the diet). The normal essential amino acids are isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, arginine, histidine, and valine.

What is Whipple's disease? How does it present and what are the treatments?

Whipple's disease typically presents with a combination of foul-smelling diarrhea, abdominal distention, joint pain, neurological and cardiac problems, as this is a systemic infection. On physical exam, there is lymphadenopathy because this is an active infection. The mesenteric lymph nodes receive lymph from the gastrointestinal tract, and the bacteria can spread to peripheral lymph nodes, which can be palpated on physical exam. Because Whipple's disease is the only answer choice that includes systemic symptoms, the other choices can be eliminated. Tropheryma whippelii is the gram positive bacterium that causes Whipple's disease. Although rare, it most commonly occurs in older Caucasian males. Once macrophages detect T. whippelii in the lamina propria of the small bowel, they attempt to destroy the bacteria by phagocytosis. On microscopic exam, we can observe foamy macrophages that stain positive with the periodic acid schiff (PAS) stain. The large amount of foamy macrophages compresses the lacteals in the villi of the small intestine, which prevents chylomicrons from entering into the lymphatic system. Since more chylomicrons cannot form due to decreased space, fat absorption is inhibited, leading to fat malabsorption and steatorrhea. Treatment involves antibiotics, such as doxycycline or macrolides.